Saphenous Vein Graft Aneurysms 

  • Author: Jesse P Jorgensen, MD; Chief Editor: Eric H Yang, MD   more...
 
Updated: Oct 4, 2011
 

Background

Coronary artery revascularization with saphenous vein grafts (SVGs) has become a surgical standard for treatment of coronary artery disease since Favaloro first described it in 1967. Riahi and associates described the rare complication of saphenous vein graft aneurysm (SVGA) in 1975.[1]

SVGA is defined as a localized dilation of the vessel to 1.5 times the expected normal diameter. These are classified as true and false aneurysms (or pseudoaneurysms): true aneurysms involve all 3 layers of the vessel wall, whereas false aneurysms involve disruption of 1 or more layers of the vessel wall with a well-defined collection of blood or hematoma outside the endothelium. Further classification of SVGAs as large or small is not well defined, although dilation to more than 2 cm has generally led to consideration for surgical therapy. SVGAs reported in literature range from 1-14 cm in diameter.

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Pathophysiology

The SVG to left anterior descending is the most common site for aneurysm formation, followed by the right coronary artery, and least commonly, the left circumflex.

True aneurysms, which usually develop in the body of the vein graft and are typically fusiform, are usually the result of a chronic, degenerative process caused by vascular injury that results from hyperlipidemia and progression of atherosclerosis. The initial event in SVGA formation is thought to be atheroma formation followed by plaque rupture, resulting in injury to the vessel wall, which is exacerbated by arterial pressures within the vein graft. Valve insertion points along the vein graft are especially prone to true SVGA formation, where smooth muscle in the media changes from circular to a weaker longitudinal orientation. Other possible contributing factors include varicosities with impaired elastic tissue integrity not detected at the time of harvesting, vascular injury from previous percutaneous intervention (PCI), and surgical trauma.

False aneurysms are saccular and typically located at the proximal SVG anastomosis, although they have been reported in the body and at the distal anastomosis. These are thought to occur because of tension on the anastomosis with suture rupture, or from technical issues in suture placement. Infection, particularly postoperative mediastinal sepsis involving Staphylococcus aureus, is commonly associated with false aneurysm formation because of suture line dehiscence. SVGA formation in the body of the graft has been reported to occur at the site of previous PCI and in the setting of chronic corticosteroid use.

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Epidemiology

Frequency

International

Mild aneurysmal dilation of SVGs is relatively common, with a frequency of approximately 14% within 5-7 years of surgery.

A literature review from the first reported case in 1975 until 2002 revealed 50 true aneurysms and 26 false aneurysms. In a review of all bypass cases at one institution from 1975-1991, of 1658 patients with 5579 grafts, 4 developed SVGA, giving an incidence of 0.07%. The incidence of significant SVGA is probably underestimated because the initial presentation may be rupture leading to sudden death, the aneurysm may not appear on angiography if it contains significant thrombus, and many patients are asymptomatic.

Mortality/Morbidity

  • SVGA rupture is associated with high morbidity and mortality rates.
  • Ischemic symptoms, either angina or infarction, can occur from graft occlusion, embolic phenomena, or compression of the graft by the aneurysm. Many SVGAs cause no symptoms and remain subclinical; thus, morbidity and mortality estimates are likely affected by a selection bias.
  • In symptomatic patients, the mortality rate is high, with 13 of 46 patients (28%) dying within 90 days of initial symptoms.

Race

Among reported cases in which race was identified, the patients were white. This may reflect a selection bias.

Sex

SVGAs are more common in men than women. In the literature review cited above, 64 of the 76 patients (84%) were men; this may be, in part, because more men than women undergo coronary artery bypass surgery.

Age

The average age of patients at the time of diagnosis is 59 years (range, 23-80 y).

  • Women tend to be older than men at presentation, probably because they tend to develop coronary artery disease later in life and therefore undergo coronary artery revascularization later.
  • Patients with SVGA typically present years after surgery, with 10-20 years as the average time to onset; however, both true and false SVGAs have been reported within months of surgery.
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Contributor Information and Disclosures
Author

Jesse P Jorgensen, MD  Fellow, Department of Cardiology, Emory University School of Medicine

Jesse P Jorgensen, MD is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

Tarek Helmy, MD, FACC  Assistant Professor of Clinical Medicine, Division of Cardiovascular Diseases, University of Cincinnati School of Medicine

Tarek Helmy, MD, FACC is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, and American Heart Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Craig T Basson, MD, PhD  Gladys and Roland Harriman Professor of Medicine, Director of the Center for Molecular Cardiology, Director of Cardiovascular Research, Division of Cardiology, Department of Medicine, Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital

Craig T Basson, MD, PhD is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Steven J Compton, MD, FACC, FACP  Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD  Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program, Henry Ford Hospital

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Christian Birkedal, MD and J Thomas Williams, MD to the development and writing of this article.

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CT scan demonstrating a saphenous vein graft aneurysm.
Cardiac catheterization demonstrating a saphenous vein graft aneurysm.
Aortogram demonstrating a saphenous vein graft aneurysm.
This CT scan reveals a saphenous vein graft aneurysm.
Angiogram of a saphenous vein graft to the distal right coronary artery demonstrating a large aneurysm in the mid portion of the graft. Video courtesy of John S. Douglas, MD.
Final angiogram demonstrating coils within the aneurysm, and almost complete cessation of flow from the parent vessel into the aneurysm. Video courtesy of John S. Douglas, MD.
Another view demonstrating the saphenous vein graft aneurysm. Video courtesy of John S. Douglas, MD.
The first of many coils being deployed in the aneurysm. Video courtesy of John S. Douglas, MD.
 
 
 
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